1. Description of the problem

What every clinician needs to know

Acute kidney injury in the child/newborn is defined as an abrupt cessation or diminution of kidney function. The time frame for pediatric AKI is now considered to be less than 48 hours. Multi-dimensional pediatric AKI definitions include the pediatric modified RIFLE criteria (pRIFLE: Risk, Injury, Failure, Loss, End-stage kidney disease) and the Acute Kidney Injury Network (AKIN criteria).

Clinical features

The clinical features of AKI include:

Oliguria

Hyperkalemia

Acidosis

Volume overload

Hypertension

Hyperphosphatemia

Uremia

Hypocalcemia

Key management points

The key management points for pediatric AKI include, in order of importance:

Treat life-threatening features of pediatric AKI with medical management or renal replacement therapy (dialysis). These include:

3. Diagnosis

Diagnostic criteria and tests

The diagnosis of AKI is based on increases in serum creatinine or decreases in urine output. Until recently, multiple diagnostic criteria were used, which confounded analysis. Recent validation of the pediatric modified RIFLE (pRIFLE) criteria has standardized the definition and diagnosis of AKI presence and severity.

pRIFLE creatinine-based AKI criteria: Serum creatinine values are used to calculate an estimated creatinine clearance (eCCl) by the Schwartz formula:

eCCl (ml/min/1.73m2) = k * patient height (cm)/serum creatinine (mg/dl), where k is a constant based on patient’s gender and age

k values: low birth weight less than 1 year (0.33); full term less than 1 year (0.45); 2-12 years of age (0.55); 13-21 year old female (0.55); 13-21 year old male (0.70).

Use baseline and current serum creatinine to calculate a change in eCCl.

If no baseline serum creatinine is available for 3 months prior to current value, assume eCCl = 120 ml/min/1.73m2.

pRIFLE urine output-based criteria: At least 8 hours of recorded UOP is required to diagnose AKI with the pRIFLE UOP-based criteria.

pRIFLE AKI strata: less than 0.5 ml/kg/hour for 8 hours (pRIFLE-R); less than 0.5 ml/kg/hour for 16 hours (pRIFLE-I); less than 0.3 ml/kg/hour for 24 hours or anuric for 12 hours (pRIFLE-F).

Normal lab values

The normal serum electrolyte and creatinine ranges vary by pediatric patient age as a result of nephron tubular maturation. Table I lists the general ranges based on patient age. These should serve only as one piece of data to inform clinical decision-making, as many electrolyte concentrations can be affected by dietary and other non-kidney-function-related factors.

Table 1.

Infant

Child

Adolescent

Sodium (meq/L)

130-140

133-146

133-146

Potassium (meq/L)

3.7-5.9

3.4-4.7

3.5-5.1

Chloride (meq/L)

98-113

98-107

98-107

Bicarbonate (meq/L)

16-24

22-26

22-26

Blood urea nitrogen (mg/dL)

< 20

< 20

<20

Creatinine (mg/dL)

0.2-0.4

0.3-0.7

0.5-1.0

Calcium (mg/dL)

9.0-11.0

8.8-10.8

8.6-10.0

Phosphorus (mg/dL)

4.5-6.7

4.5-5.5

2.7-4.5

Magnesium (mg/dL)

1.3-2.0

1.3-2.0

1.3-2.0

Uric acid (mg/dl)

2.4-6.4

2.4-5.9

2.4-7.2

Urine output

Typically, urine output is reported in terms of ml/kg of patient body weight/hour, with a value greater than 1 ml/kg/hour considered to be “normal.”

In AKI, the 1ml/kg/hour threshold does not apply as patients may have a “relative oliguria” if they have received large fluid volumes, which would require sufficiently greater urine volumes to maintain euvolemia.

Thus, matching intake to output and assessing daily weight and edema status are crucial to determine if urine output is really “normal”.

Establishing a diagnosis

You know that the patient has AKI if he/she has sustained periods of oligo-anuria and/or some of the metabolic derangements noted above.

The pRIFLE diagnostic criteria serve as a guideline to detect AKI and to determine its severity in children.

Other possible diagnoses

The differential diagnosis for pediatric AKI mainly focuses on the potential cause of AKI. These causes have classically been characterized as pre-renal, intrinsic renal and post-renal.

Post-renal disease: Results from obstruction to urinary flow from the level of the renal pelvis to the urethra. These entities can be congenital or acquired. The obstruction usually must be bilateral (above the level of the urethra) to cause kidney failure.

Causes

Congenital

Posterior urethral valves (males only).

Ureteral-vesical junction obstruction.

Ureteral-pelvic junction obstruction.

Severe vesico-ureteral reflux.

Eagle-Barrett (prune-belly) syndrome.

Acquired

Trauma.

Oncologic lesions (neuroblastoma, Wilms’ tumor most common).

Nephrolithiasis with obstructing stones.

Ureteral/urethral/bladder clots.

Confirmatory tests

The following lab and radiologic tests should be considered in patients with suspected acute kidney injury:

Drugs and dosages

The drug dosages listed here are for guidance only as few randomized trials have compared efficacy of different regimens in children. For doses of vasoactive and inotropic medications, please refer to the chapter on “Septic Shock” in this section.

Direct toxic effect to the proximal tubules by an exogenous or endogenous toxin.

In either case, damage to the proximal tubule can lead to tubule cell sloughing into the proximal lumen, with obstruction to urinary flow and backleak though the tubules and into the glomerulus. Once the injury has subsided, the proximal tubules must regenerate their integrity and polarity to resume normal function.

Epidemiology

The epidemiology of pediatric acute kidney injury has changed from the 1990s on from primary kidney disease to another system illness or its treatment.

Only 7% of pediatric acute kidney injury cases result from a primary kidney disease in the tertiary hospitalized setting. In the intensive care setting, multi-organ dysfunction syndrome, with primary cardiac, hepatic, hematological or pulmonary diagnoses, is the most common. Pediatric acute kidney injury affects the entire pediatric age spectrum, from premature neonates to young adults.

Prognosis

Children admitted to an ICU have worse survival rates than those who are not.

Critically ill children receiving invasive mechanical intubation and on vasoactive medication have an independent increased risk of mortality if they experience pRIFLE-I or pRIFLE-F acute kidney injury compared to no acute kidney injury or pRIFLE-R AKI.

Children with acute decompensated heart failure have an independent increased risk of death or requirement for a cardiac mechanical assist device if they experience a serum creatinine rise greater than or equal to 0.3 mg/dl.